Q-omics provides the consensus-scored CAMKMT profile across patient tissues and cancer cell-line models. CAMKMT expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UCS. Among the 18 cancer types available for tumor–normal comparison, CAMKMT is differentially expressed in 15, with the highest sampling consensus in KICH. Additionally, CAMKMT RNA expression shows 19,362 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UCS, KICH, and UVM as cancer lineages where CAMKMT shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for CAMKMT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CAMKMT survival associations across molecular data types. CAMKMT RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CAMKMT RNA expression–survival associations across cancer types. High CAMKMT expression shows unfavorable associations in UCS, LGG, BLCA, ACC and SKCM, but favorable associations in KIRC. The UCS Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify UCS as the clearest survival context for CAMKMT RNA expression.
This table summarizes CAMKMT tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 2. The strongest signals are observed in KICH for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for CAMKMT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CAMKMT shows lower tumor expression in KICH, KIRC and THCA and higher tumor expression in COAD, STAD and LIHC. The KICH box plot shows higher CAMKMT RNA expression in normal versus tumor tissue (log2 FC = −2.206, t-test p < 0.001).
This table shows molecular features associated with CAMKMT in patient tissues and cancer cell lines. In patient samples, CAMKMT shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CAMKMT RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and UPPER_AERODIGESTIVE_TRACT.
